We propose to study basic human decision making mechanisms of sensory integration, hypothesis testing and response selection. We also propose to study the control mechanisms necessary for modulating these decision making processes in response to varying task conditions. We propose to investigate these mechanisms using event-related encephalography (EEC) and functional magnetic resonance imaging (fMRI) to complement our existing behavioral results. The major questions that we propose to address are whether a simple "leaky competing accumulator" (LCA) model of the neural circuitry underlying perceptual decision making in non-human primates is implemented in the human brain;and if so, whether evidence exists for an extension which we have developed of this model that can account for adaptations of performance associated with cognitive control -a disturbance of which is central to most forms of psychiatric disorder. A simple LCA model of sensory integration and hypothesis testing that is supported by direct neuronal recordings in non-human primates suggests that neurons in the lateral intraparietal sulcus (area LIP) implement an evidence-weighing process in the context of motion-discrimination tasks requiring eye-movement responses. Furthermore, this activity is modulated by the expected reward associated with possible outcomes. Our hypothesis is that these phenomena reflect three general, cross-species principles that govern all response modalities in most tasks: 1) stimulus-response associations are implemented in the brain at intermediate stages of processing that transform the outputs of stimulus identification stages into response initiation;2) ramping activity in these initial stages of the response channels reflects not only the advance preparation of anticipated movement features prior to a response, but also - critically - it reflects the actual weighing of evidence about which response to make;3) cognitive control in its simplest form is implemented at this stage by modulating the threshold applied to this evidence on the basis of continuous reward and cost monitoring. We propose to test this hypothesis using a motion-discrimination task involving two response modalities and multiple manipulations of reward contingency. This task is well suited for aligning our noninvasive results with direct recording data, and the model we have developed of circuits involved in this task allow strong, quantitative predictions about the temporal profile of activation in all of the model's components. This task may provide a window into the process by which disturbances of affect resulting from injury or psychiatric disease lead to disturbances of basic cognitive processing through inappropriate threshold control. It may also explain how control deficits lead to impaired reward processing.